The present invention is directed to a medical product which can be used to correct vision loss or blindness caused by certain retinal diseases. A variety of retinal diseases cause vision loss or blindness by destruction of the choroid, choriocapillaris, and the outer retinal layers of Bruch's membrane and retinal pigment epithelium. Loss of these layers is followed by degeneration of the inner retinal photoreceptor layer. As severe as the disruption of the outer retina usually is, the remaining inner retina (composed of the outer nuclear, outer plexiform, inner nuclear, inner plexiform, ganglion cell and nerve fiber layers) may be spared. The sparred inner retina can be utilized, in combination with devices that perform the function of the damaged photoreceptor cells, to restore vision.
Prior efforts to produce vision by stimulating various portions of the retina have been reported. One such attempt involved an externally powered, but internally located, photosensitive device with opposing photo-active and electrode surfaces. The device would theoretically stimulate the nerve fiber layer by its direct placement upon this layer from the vitreous body. The success of this device is questionable, however, due to the complex frequency modulated neural signals of the nerve fiber layer that the device must duplicate. Further, the normal nerve fiber layer runs in a general radial course with many layers of overlapping fibers appearing from different portions of the retina. Selection of the appropriate nerve fibers to stimulate in order to produce formed vision, therefore, would be extremely difficult, if not impossible.
Another prior device involved a unit consisting of a supporting base onto which a photosensitive material such as selenium was coated. This device was designed to be inserted through an external scleral incision made at the posterior pole of the eye. The device would rest between the sclera and choroid, or between the choroid and retina. Light would cause a potential to develop across the photosensitive surface producing ions that would theoretically migrate into the retina causing stimulation. However, having no discrete surface structure to restrict the directional flow of charges, lateral migration and diffusion of charges would occur thereby preventing sufficient image resolution to be developed. One such device was reportedly constructed and implanted into a patient's eye resulting in light perception, but not formed imagery.
Placement of this device between the sclera and choroid would also result in blockage of discrete ion migration to the photoreceptor and inner retinal layers. This effect is due to the intervening presence of the choroid, choriocapillaris, Bruch's membrane and the retinal pigment epithelial layer--all of which would block passage of these ions. Placement of the device between the choroid and the retina would still interpose Bruch's membrane and the retinal pigment epithelial layer in the pathway of discrete ion migration. As this device would be inserted into or through the highly vascular choroid of the posterior pole, subchoroidal, intraretinal and intraorbital hemorrhaging would likely result along with disruption of blood flow to the posterior pole.
U.S. Pat. Nos. 5,016,633 and 5,024,223, both issued to the present inventor (the contents of which are hereby incorporated by reference), also reported a design for a subretinally placed photoelectric device comprised of multiple surface electrode microphotodiodes (SEMCP's) deposited on a single silicon crystal substrate. These SEMCP's transduce light, passing through a semitransparent electrode surface and onto a photo-active surface, into small electric currents that stimulate overlying and surrounding inner retinal cells. However, due to the solid nature of the substrate onto which the SEMCP's were placed, blockage of nutrients from the choroid to the inner retina likewise occurs. Even with fenestrations of various geometries, permeation of oxygen and biological substances is not optimal.